Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Addition of dimethylsulfoxide at concentrations of 1% and 2% (vol/vol) to cells of mouse neuroblastoma clone NIE-115 in the confluent phase of growth resulted in the production of morphologically differentiated cultures with extensive process formation. Cell maintained in 2% dimethylsulfoxide remained in a stable nondividing condition for periods of up to 4 weeks. A high degree of electrical excitability was found in these cells, but there was no clear correlation of this property with the level of induction of either acetylcholinesterase (acetylcholine hydrolase; EC 3.1.1.7) or tyrosine hydroxylase [L-tyrosine, tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating); EC 1.14.16.2]. In addition, intracellular levels of cyclic 3':5'-AMP were not elevated in fully morphologically and electrically differentiated cells. While cell division was markedly inhibited by 2% or higher concentrations of dimethylsulfoxide, at 1% growth continued at a somewhat slowed rate and such cultures exhibited enhanced process formation and electrical activity for a relatively short period. High concentrations (3% or 4%) of dimethylsulfoxide totally suppressed process formation and did not result in increased excitability, but cells maintained high resting potentials. The results suggest that the development of the excitable membrane in neuroblastoma cells may be expressed independently of neurospecific enzyme induction, and does not require a sustained elevation of cyclic 3':5'-AMP levels.
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PMID:Maturation of neuroblastoma cells in the presence of dimethylsulfoxide. 0 56

Cell division, neurite formation and acetylcholinesterase activity were examined in a clone (NBA2) of mouse neuroblastoma cells maintained for up to 120 hours in medium with pH values between 6.6 and 8.0. Growth rate decreased as pH was reduced from 7.8 to 6.6. Generation time at pH 7.4 was 25 hours, while the rate of cell division was negligible at pH 6.6. The total number of cells at stationary phase was less at the lower pH values. Neurite formation was enhanced markedly as the pH was reduced from 7.4 to 6.6. Acetylcholinesterase activity was 5- to 8-fold greater in cells exposed to medium at pH 6.6 than in cells maintained in medium at pH 7.4. The reduction in the rate of cell division and increases in neurite formation and acetylcholinesterase activity at pH 6.6 were reversible upon exposure of the cells to pH 7.4 medium. Cell viability was greater than 90% at all medium pH values over a period of 120 hours. Uncloned T-59 mouse neuroblastoma cells were affected similarly by changes in pH. These results show that manipulation of the environmental pH can reversibly alter growth, neurite formation, and acetylcholinesterase activity of mouse neuroblastoma cells in culture.
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PMID:The effect of medium pH on rate of growth, neurite formation and acetylcholinesterase activity in mouse neuroblastoma cells in culture. 1 20

A variety of compounds were assessed for their ability to induce morphological differentiation and to affect the synthesis of RNA in uncloned mouse neuroblastoma cells in culture. The stimulation of morphological differentiation in uncloned cells after exposure for 48 hours to concentrations of 3 times 10-7 to 3 times 10-4 M papavarine or 10-9 to 10-3 M dibutyryl adenosine 3':5'-monophosphate (dibutyryl-cAMP) was associated, in part, with a concentration-dependent decrease in incorporation of [5-3H]uridine into ribosomal RNA (rRNA) and heterogeneous RNA (HnRNA). The latter effect on cellular RNA produced by papavarine occurred within 1 hour after its addition to the medium and was associated with impaired uptake of radioactive precursor into uridine nucleotides and reduction in the intracellular concentration of uridine 5'-triphosphate (UTP). Dibutytyl-cAMP produced a decreased in the specific radioactivity of UTP without affecting the concentration of UTP in the tumor cells. The effects of papavarine and dibutyryl-cAMP could be distinguished further by the 50% reduction of acetylcholinesterase activity produced by papavarine, but not by dibutyryl-cAMP. Papavarine did not, however, reduce the cellular level of the soluble enzyme, adenine phosphoribosyltransferase. Sodium butyrate, while producing morphological effects similar to those of papavarine and dibutyryl-cAMP at equimolar concentrations, caused no significant changes in the incorporation of [5-3H]uridine into rRNA and HnRNA; however, acetylcholinesterase activity was stimulated 6- to 7-fold above control levels. In contrast to the other differentiating agents examined, addition of 10-9 to 3 times 10-4 M concentrations of cAMP to the tissue culture medium enhanced morphological differentiation of nueroblastoma cells, and caused a 10- to 20-fold stimulation of the incorporation of [5-3H]uridine into rRNA and HnRNA at concentrations of 10-4 M and higher. This effect observed only at high concentrations of cyclic nucleotide was accompanied by an elevation in the specific acitivty of UTP, These studies suggest that the morphological response of neuroblastoma cells is not necessarily associated with concomitant alterations in the synthesis of RNA with agents other than cAMP. Observed changes in incorporation of [5-3H]uridine into RNA appear in most instances to be due to alterations in the uptake of uridine, and in the pool size and specific radioactivity of UTP.
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PMID:Effects of adenosine 3':5'-monophosphate and related agents on ribonucleic acid synthesis and morphological differentiation in mouse neuroblastoma cells in culture. 16 51

Removal of sialic acid from intact mammalian nervous system cells in tissue culture is accompanied by an immediate increase in cellular cholinesterase activity. Treatment of hamster astroblast cells (clonal line NN) and mouse neuroblastoma cells (clonal lines S21, N18, and N115) for brief periods with a low level of Clostridium perfringens sialidase, 5 X 10(-3) units/ml, removed 1-15 mug of sialic acid per mg of cell protein and brought about a large increase in v0 and Vmax of cellular acetylcholinesterase (EC 3.1.1.7). Butyrylcholinesterase (EC 3.1.1.8) activities also increased upon careful enzymatic removal of cellular sialic acid, and cells with characteristically low butyrylcholinesterase activity, e.g., adrenergic clonal line N115 neuroblasts displayed relatively high activity after treatment with sialidase. These findings open the possibility that adaptive regulation of cholinesterases in mammalian cells may be mediated rapidly through changes in their sialic acid content.
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PMID:Activation of acetyl- and butyrylcholinesterase by enzymatic removal of sialic acid from intact neuroblastoma and astroblastoma cells in culture. 17 21

The release of acetylcholinesterase from neurons was studied using cultured chick-embryo spinal-cord cells. Cells dissociated from 12-day-old chick-embryo spinal cords were grown in culture for 10-12 days. Numerous well differentiated spinal neurons were found after 7-10 days in culture. Acetylcholinesterase activity per dish increased by 60-fold from days 2-12. Acetylcholinesterase was released into the surrounding media by the cells when they were incubated either in the standard culture medium or the serum-free medium. Acetylcholinesterase release was significantly reduced when protein synthesis and microtubules were disrupted by cycloheximide and colchicine, respectively. Histochemical localization of acetylcholinesterase indicated that the synthesis and relase of acetylcholinesterase are attributable to neurons. Cultured chick-embryo brain and neuroblastoma cells also released acetylcholinesterase into the media. These results are discussed with regard to possible physiological roles for acetylcholinesterase secretion from neurons.
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PMID:Release of acetylcholinesterase by cultured spinal cord cells. 56 29

In the presence of 1--2% dimethyl sulfoxide (DMSO), mouse neuroblastoma cells are induced to differentiate morphologically as well as electrically. In addition, treatment of neurolbastoma cells with 2% DMSO results in a marked increase in the veratridine-activated K+ or Rb+ efflux. At 4% DMSO, neurite outgrowth is completely repressed and electrical activity is poorly developed. However, at this concentration, the cells have a relatively high resting potential which suggested that membrane components determining passive and active permeability properties are not necessarily under coordinated control. Induction of differentiation by 2% DMSO is also accompanied by an increase in a heavier molecular form of acetylcholinesterase sedimenting at 10.5S. The effect of other agents on the growth and differentiation of neuroblastoma cells is also presented.
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PMID:Induction of differentiation in mouse neuroblastoma cells. 74 53

Mouse neuroblastoma clone NIE-115 contains two species of acetylcholinesterase (AChE) which sediment at 4S and 11S. The former is predominant in growing cells (70%), whereas the 11S is more abundant in cells with neurites (55--65%). When cell replication is arrested by sodium butyrate, there is an increase in AChE activity but no modification in the proportion of 4S:11S species. Inhibition of protein synthesis by cycloheximide provokes a slow increase in the 11S form and a parallel decrease in 4S. Neurite retraction in presence of colchicine or excess serum does not lead to a concomitant reversion in the high 11S proportion. We postulate that the 11S AChE is formed by a conversion of the 4S and that the shift in the S-value ratio of the enzyme reflects changes in membrane remodeling during neurite extension.
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PMID:Phenotypic modulation in mouse neuroblastoma cells: the case of acetylcholinesterase. 74 57

When mouse neuroblasts (clonal line M 1) and hamster astroblasts (clonal line NN) were co-cultured, the originally low activity of acetylcholinesterase of both lines was drastically increased. After 2 months the neuroblastoma M 1 cells were reisolated from the co-culture and were found to contain 10 times higher activity of acetylcholinesterase than the original M 1 cells. This increased activity was maintained over more than 14 subcultures. In contrast, co-cultivation of neuroblastoma M 1 cells with rat astrocytoma cells (clonal line C 6) resulted in a decrease of actylcholinesterase activity compared to either original cell line.
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PMID:[Acetylcholinesterase activity of neuroblastoma and different glial cells in co-culture]. 81 44

Cells of three established lines of human neuroblastoma and an established line of C1300 mouse neuroblastoma were grown in control medium or in experimental medium containing mouse nerve growth factor (NGF). Cultures were stained histochemically for acetylcholinesterase (AChE) during log growth and at confluency. Human neuroblastoma cells grown in medium containing NGF were morphologically more differentiated and they were stained much more intensely for AChE during both phases of growth than were cells in control cultures. The enzyme was distributed over cell bodies and neurites. Neuroblastoma cells of the mouse line were not stimulated to form neurites by NGF, but they were more intensely stained for acetylcholinesterase than cells grown in control medium. These observations support earlier findings that NGF stimulates differentiation of human and mouse neuroblastoma cells in vitro.
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PMID:Histochemical demonstration of an increase in acetylcholinesterase in established lines of human and mouse neuroblastomas by nerve growth factor. 103 92

The techniques of somatic cell hybridization allow a genetic analysis of differentiated functions of mammalian cells in vitro. Clonal lines of mouse neuroblastoma cells expressing a variety of differentiated neuroectodermal functions have been fused to L cells not expressing these functions. The resulting NL hybirds, on a clonal basis, express a variety of parental and non-parental phenotypes. Some hybrid clones inherit the ability to synthesize the neurotransmitter acetylcholine (Ach) (expression of high levels of choline acetyltransferase, CAT) while others do not. The ability to synthesize Ach and the ability to degrade this neurotransmitter (high levels of acetylcholinesterase activity, AChE) appear to segregate independently in NL hybrid progeny.--When a a variety of clonal cell lines replicating in culture are fused to cells freshly derived from the embryonic nervous system, interesting phenotypes result in the hybrid progeny. Neuroblastoma x rodent nervous tissue hybrids express AChE and in a few instances have developed the ability to synthesize CAT. Transformed human fibroblasts fused to normal rodent nervous tissue yield hybrid progeny that retain human and segregate mouse chromosomes and isozymes. No expression of differentiated functions has yet been found in these latter hybrids but they are useful for mapping mouse genes.
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PMID:Expression of phenotypes in hybrid somatic cells derived from the nervous system. 115 88


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